The hypothesis of this study is that vitamin D binding protein (DPB) is an essential component of the actin scavenging system. Oversaturation of the binding capacity of DPB for actin may result in intravascular polymerization of G-actin to F-actin, leading to F-actin deposition in the in the microvasculature, with subsequent endothelial cell injury, microthrombi, and vascular obstruction. The specific aim of the study is to determine if oversaturation of the capacity of plasma DBP to bind G-actin results in deposition of F-actin in the circulation and the resultant formation of microthrombi resulting in ARDS. This study combines patient -oriented research, utilizing the resources of the GCRC, with the most up-to-date techniques in molecular biology, by which mouse models of DPB deficiency (gene targeting) and DPB excess (trangenic mice) will be generated.